Objectives: . The annual prevalence of chronic rhinosinusitis (CRS) is increasing, and the lack of effective treatments imposes a substantial burden on both patients and society. The formation of nasal polyps in patients with CRS is closely related to tissue remodeling, which is largely driven by the epithelial-mesenchymal transition (EMT). MicroRNA (miRNA) plays a pivotal role in the pathogenesis of numerous diseases through the miRNA-mRNA regulatory network; however, the specific mechanism of the miRNAs involved in the formation of nasal polyps remains unclear. Methods: . The expression of EMT markers and Smad3 were detected using western blots, quantitative real-time polymerase chain reaction, and immunohistochemical and immunofluorescence staining. Differentially expressed genes in nasal polyps and normal tissues were screened through the Gene Expression Omnibus database. To predict the target genes of miR-145-5p, three different miRNA target prediction databases were used. The migratory ability of cells was evaluated using cell migration assay and wound healing assays. Results: . miR-145-5p was associated with the EMT process and was significantly downregulated in nasal polyp tissues. In vitro experiments revealed that the downregulation of miR-145-5p promoted EMT. Conversely, increasing miR-145-5p levels reversed the EMT induced by transforming growth factor-β1. Bioinformatics analysis suggested that miR-145-5p targets Smad3. Subsequent experiments confirmed that miR-145-5p inhibits Smad3 expression. Conclusion . Overall, miR-145-5p is a promising target to inhibit nasal polyp formation, and the findings of this study provide a theoretical basis for nanoparticle-mediated miR-145-5p delivery for the treatment of nasal polyps.

Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.

Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.
Autophagy ; Brain Ischemia ; Cell Death ; Cerebral Infarction ; Humans ; Medicine, Chinese Traditional

Objective:To explore the etiology and treatment of one case of bilateral mandibular second molar impaction with paradental cyst, and to provide a reference for its diagnosis and treatment. Methods:Root canal treatment of the left mandibular first molar of the patient was performed before operation.The left mandibular second molar of the patient was removed;the residual dental follicle, the granulation tissue and the cyst wall were stroken off under local anesthesia.The diamond ball was used to polish the wound cavity and sharp bone edge, and to mill the distal apical part of left mandibular first molar.The tissue removed during the procedure was used for the pathological examination.Results:The X-ray image showed that the bilateral mandibular second molar was impacted with the left mandibular first molar root's absorption, and there was a clear round-like density reduction zone around the second molar crown.The pathologic result was paradental cyst.Conclusion:Dental impaction complicated with paradental cyst could occur in other tooth position except for the third molar.Its diagnosis should be combined with the clinical manifestations, the pathologic manifestations and the medical imaging.Multidisciplinary consultation is in favor of its diagnosis and treatment.

OBJECTIVETo investigate the effect of intensive rosuvastatin therapy on adhesion molecules in patients with peripheral atherosclerosis and explore the possible upstream mechanism.

METHODSTwenty asymptomatic patients with peripheral atherosclerosis were enrolled and given 5-20 mg/day rosuvastatin for 3 months. Before and after the treatment, the lipid profile and plasma vascular cell adhesion molecule-1 (VCAM-1) levels were examined. The expression of intercellular adhesion molecule-1 (ICAM-1) in the mononuclear cells was measured using flow cytometry, and the mRNA and protein expressions of peroxisome proliferator-activated receptor γ (PPARγ) were detected using RT-PCR and Western blotting, respectively.

RESULTSCompared with the baseline levels, ICAM-1 expression decreased and PPARγ protein expression increased in the lymphocytes. Rosuvastatin therapy did not produce obvious effects on plasma VCAM-1 level or ICAM-1 expression in the monocytes in these patients.

CONCLUSIONRosuvastatin produces anti-inflammatory effects by decreasing the expression of ICAM-1 in mononuclear cells, and its upstream mechanism may involve the PPARγ pathway.

Atherosclerosis ; drug therapy ; metabolism ; Cell Adhesion Molecules ; metabolism ; Female ; Fluorobenzenes ; administration & dosage ; therapeutic use ; Humans ; Intercellular Adhesion Molecule-1 ; metabolism ; Male ; Middle Aged ; Monocytes ; drug effects ; metabolism ; PPAR gamma ; metabolism ; Pyrimidines ; administration & dosage ; therapeutic use ; Rosuvastatin Calcium ; Sulfonamides ; administration & dosage ; therapeutic use ; Vascular Cell Adhesion Molecule-1 ; metabolism

We described the first results of a quantitative ultra performance liquid chromatographytandem mass spectrometry method for a novel antimicrobial peptide (phylloseptin,PSN-1).Chromatographic separation was accomplished on a Waters bridged ethyl hybrid (BEH) C18 (50 mm × 2.1 mm,1.7 μm) column with acetonitrile-water (25∶75,v/v) as isocratic mobile phase.Mass spectrometry detection was performed in the positive electrospray ionization mode and by monitoring of the transitions at m/z 679.6/120,509.6/120 (PSN-1) and m/z 340.7/165 (Thymopentin,IS).Protein precipitation was investigated and the recovery was satisfactory (above 82％).The method was shown to be reproducible and reliable with intra-day precision below 5.3％,inter-day precision below 14.2％,and linear range from 0.02 to 2 μg/mL with r＞0.994.The method was successfully applied to a pharmacokinetic study of PSN-1 in rats after intravenous administration.

The ubiquitin-like modifier bISG15 is an antiviral protein found in fetal bovine lung (FBL) cells.Bovine Herpesvirus 1(BHV-1),which is a viral pathogen of cattle,can infect FBL cells and induce cytopathic effects.Real-time PCR assays showed that BHV- 1 's infection could repress the basal or inducible transcription of bISG15 in FBL cells.It demonstrates that this repression effect depends on BHV-1 viral infection and new protein synthesis.Our previous work showed that bIRF-3 was the key factor in the stimulation of bISG 15 in FBL cells,so the effect of BHV-1 viral protein on bIRF-3 activating the promoter of bISG15 was confirmed.The luciferase assay showed the BHV-1 viral protein bICP0 inhibited the activation of bISG15 promoter stimulated by bIRF-3.Taken together,our work suggested that BHV-I had some molecular mechanism to resist the cellular bISG15'santiviral functions.

We described the first results of a quantitative ultra performance liquid chromatographytandem mass spectrometry method for a novel antimicrobial peptide （phylloseptin, PSN-1）. Chromatographic separation was accomplished on a Waters bridged ethyl hybrid （BEH） C18 （50mm× 2.1 mm, 1.7 μm） column with acetonitrile-water （25：75, v/v） as isocratic mobile phase. Mass spectrometry detection was performed in the positive electrospray ionization mode and by monitoring of the transitions at m/z 679.6/120, 509.6/120 （PSN-1） and m/z 340.7/165 （Thymopentin, IS）. Protein precipitation was investigated and the recovery was satisfactory （above 82%）. The method was shown to be reproducible and reliable with intra-day precision below 5.3%, inter-day precision below 14.2%, and linear range from 0.02 to 2 lag/mL with r〉0.994. The method was successfully applied to a pharmacokinetic study of PSN-1 in rats after intravenous administration.

In order to quantitate the bovine immunodeficiency virus (BIV) infection in vitro, a BIV indicator cell line (BIVL) was established by transfecting baby hamster kidney cells with reporter plasmids containing the firefly luciferase gene driven by a BIV long terminal repeat promoter. The BIV activates promoter activity of the LTR to express luciferase upon infection. BIV infection could therefore by quantified by detection of luciferase activity. Compared to standard assays used to detect BIV infection, the BIVL-based assay is 10 times more sensitive than the the CPE-based assay, and has similar sensitivity with the viral capsid protein Western blot assay. BIV indicator cell line could detect BIV infection specifically. Luciferase activity of BIV infected BIVL cells showed a time dependent manner, and 60 h post infection is the optimal time to detect BIV infection. Luciferase activity of BIVL cells correlates with the BIV capsid protein expression. Moreover, a linear relationship was found between MOI and the activated intensity of luciferase expression. In brief, the BIV indicator cell line is an easy, robust and quantitive method for monitoring BIV infection.

Viruses (e.g. Human immunodeficiency virus, Human simplex virus and Prototype foamy virus) are obligate intracellular parasites and therefore depend on the cellular machinery for cellular trafficking. Bovine foamy virus (BFV) is a member of the Spumaretrovirinae subfamily of Retroviruses, however, details of its cellular trafficking remain unknown. In this study, we cloned the BFV gag gene into prokaryotic expression vector pET28a and purified the denaturalized Gag protein. The protein was used to immunize BALB/c mouse to produce antiserum, which could specifically recognize the BFV Gag protein in BFV-infected cells through western blot assay. Additionally, these results demonstrated that both the optimal and suboptimal cleavage of Gag protein occur in BFV-infected cells. Subsequently, the Gag antiserum was used to investigate subcellular localization of BFV. In immunofluorescence microscopy assays, colocalization microtubules (MTs) and assembling viral particles were clearly observed, which implied that BFV may transport along cellular MTs in host cells. Furthermore, MTs-depolymerizing assay indicated MTs were required for the efficient replication of BFV. In conclusion, our study suggests that BFV has evolved the mechanism to hijack the cellular cytoskeleton for its replication.